目的：lncRNA牛磺酸上调基因1（lncRNA TUG1）对甲状腺乳头状癌（PTC）细胞（TPC-1）增殖、凋亡和EMT进程的影响及作用机制。方法：qPCR检测人PTC组织（2019年5月至2021年4月期间在河北省唐山市工人医院手术切除的35例PTC组织及对应癌旁组织标本）与人PTC细胞TPC-1、BHP10-3、K1、SW-1736及人正常甲状腺上皮Nthyori 3-1细胞中lncRNA TUG1的表达。体外培养 TPC-1 细 胞 ，将 其 分 为 对 照 组 、si-NC 组 、si-TUG1 组 、miR-NC 组 、miR-524-5p mimic 组 、si-TUG1+NC inhibitor组、si-TUG1+miR-524-5p inhibitor 组、miR-524-5p mimic+pcDNA 组、miR-524-5p mimic+pcDNABRAF）组，对细胞进行si-TUG1、miR-524-5 pmimic、miR-524-5p inhibitor、pcDNA BRAF和各自相应的对照质粒转染，采用CCK-8法、FCM法分别检测TPC-1细胞增殖、凋亡情况；WB法检测TPC-1细胞中BRAF、PCNA、Caspase-3、E-cadherin、N-cadherin和vimentin的表达，双荧光素酶报告基因实验验证miR-524-5p与lncRNA TUG1、BRAF的靶向关系。结果：lncRNA TUG1在PTC组织及细胞中呈高表达（均P<0.05）；敲减lncRNA TUG1表达或上调miR-524-5p表达可显著抑制TPC-1细胞增殖及EMT，促进细胞凋亡（均P<0.05）；双荧光素酶报告基因实验显示，lncRNA TUG1与BRAF、miR-524-5p之间存在靶向关系；抑制miR-524-5p表达可逆转敲减lncRNA TUG1表达对TPC-1细胞的增殖、EMT进程的抑制及对其凋亡的促进作用（均P<0.05），上调BRAF表达可逆转过表达miR-524-5p对TPC-1细胞增殖、EMT的抑制及对其凋亡的促进作用（均P<0.05）。结论：lncRNA TUG1在PTC组织与TPC-1细胞中呈高表达，敲减lncRNA TUG1表达可通过miR-524-5p/BRAF轴抑制PTC细胞的增殖与EMT进程，并促进TPC-1细胞凋亡。

Objective: To investigate the effects of long non-coding RNA (lncRNA) taurine up-regulated gene 1 (TUG1) on the proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) of papillary thyroid carcinoma (PTC) cells and its mechanism. Methods: Real-time fluorescent quantitative PCR (qPCR) was used to detect the expression of lncRNA TUG1 in 35 pairs of PTC tissue and corresponding paracancerous tissue specimens that were surgically resected in Tangshan Workers’Hospital, Hebei Province from May 2019 to April 2021, human PTC cell lines (TPC-1, BHP10-3, K1, SW1736) and human normal thyroid epithelial Nthyori 3-1 cells. TPC-1 cells were cultured in vitro and divided into control group, si-NC group, si-TUG1 group, miR-NC group, miR-524-5p mimic group, si-TUG1+NC inhibitor group, si-TUG1+miR-524-5p inhibitor group, miR-524-5p mimic+pc-DNA group, and miR-524-5p mimic+ pcDNA BRAF (V-raf murine sarcoma viral oncogene homolog B1) group by transfecting corresponding vectors. CCK-8 and FCM methods were used to detect the proliferation and apoptosis of TPC-1 cells, WB method was used to detect the expression of BRAF, proliferating cell nuclear antigen (PCNA), cysteine protease-3 (Caspase-3), E-cadherin, N-cadherin and vimentin in TPC-1 cells, and the dual-luciferase reporter gene experiment was used to verify the targeting relationship between miR-524-5p and lncRNA TUG1 as well as BRAF. Results: lncRNA TUG1 was up-regulated in PTC tissues and cells (P<0.05). Silencing the expression of lncRNA TUG1 or up-regulating the expression of miR-524-5p could significantly inhibit the proliferation and EMT, and promote apoptosis of TPC-1 cells (all P<0.05). Dual-luciferase reporter gene experiment showed that there was a targeting relationship between miR-524-5p and lncRNA TUG1 as well as between miR-524-5p and BRAF (all P<0.05). Silencing the expression of miR-524-5p could reverse the effects of lncRNA TUG1 knockdown on inhibiting proliferation and EMT and promoting apoptosis of TPC-1 cells (all P<0.05), and up-regulation of BRAF expression could reverse the effects of miR-524-5p overexpression on inhibiting proliferation, EMT and promoting apoptosis of TPC-1 cell (all P<0.05). Conclusion: lncRNA TUG1 is up-regulated in PTC tissues and TPC-1 cells. Silencing the expression of lncRNA TUG1 can inhibit proliferation and EMT but promote cell apoptosis of PTC cells by regulating the miR-524-5p/BRAF axis.

R736.1; R730.2